The regulation of sodium excretion by the kidneys occurs through a variety of neural, humoral, and intrarenal regulatory mechanisms. Closure of an arteriovenous (AV) fistula produces profound decreases in cardiac output and heart rate, and electrolyte excretion by the kidneys increases. Since these same changes occur after acute unilateral nephrectomy (AUN), this maneuver has been interpreted as analogous to closure of an AV fistula. The mechanisms by which these changes are brought about will be examined in the proposed work. The role of the renal nerves in effecting the renal response to closure of an AV fistula will be studied. The effect of inhibition of prostaglandin synthesis with indomethacin or meclofenamate will be studied. The relationship of the hemodynamic changes which occur after AUN or following closure of an AV fistula to the increased electrolyte excretion will also be examined. These experiments should extend our understanding of the control of sodium balanced and have implications for disease states such as congestive heart failure and hypertension.